High-dose testosterone enanthate supplementation boosts oxidative stress, but exerts little effect on the antioxidant barrier in sedentary adolescent male rat liver
Abstract:(Sub)chronic supplementation of sedentary adolescent male rats with high TE doses does not exert a lasting major effect on the liver antioxidant barrier and redox homeostasis.
“…The higher TE dose significantly lowered BW gain and LW as compared to those in TE-untreated EndTr rats, but caused no substantial shift in the LW/BW ratio (−5%, p = 0.66) and thus no apparent hepatotoxicity in EndTr rats. Earlier, we found a significantly reduced LW/BW ratio in high-dose TE-treated adolescent UTr rats (Sadowska-Krępa et al, 2017), which may have been due to the start of TE treatment at a younger age. The training was performed at an intensity that allows maximal fat oxidation (Purdom et al, 2018), and the mean BW gains were less in all three EndTr groups than in the respective UTr groups, see Sadowska-Krępa et al (2017).…”
Section: Discussionmentioning
confidence: 55%
“…All biochemical determinations in blood serum and liver samples, except for serum lipids that were not determined before, were performed as described earlier (Sadowska-Krępa et al, 2017). Specifically: The total serum testosterone (TT) level was assessed with a DSL-4100 Testosterone RIA Kit (Diagnostic Systems Laboratories, Webster, TX, USA).…”
Section: Assay Methodsmentioning
confidence: 99%
“…All other data were analyzed by a one-way ANOVA with weekly TE dose as the main factor, followed by the Tukey test when appropriate. Comparisons with data from our previous study (Sadowska-Krępa et al, 2017) were made using Student's t -test for independent variables, as indicated in the text. Associations between variables were assessed using the Spearman rank correlation test.…”
Section: Endtr Endtr+te8 Endtr+te80mentioning
confidence: 99%
“…Our earlier study on the effects of long-term testosterone treatment on the liver antioxidant barrier and some blood markers of liver injury in sedentary adolescent male rats showed some signs of enhanced liver oxidative stress and toxicity but no potential lasting harm (Sadowska-Krępa et al, 2017). Here, we tested the possible harmful effects of this treatment in a situation aimed to model androgen abuse to aid physical exercise training.…”
In some countries, anabolic-androgenic steroid abuse is rampant among adolescent boys and young men, including some of those seeking physical fitness and/or pleasing appearance through various exercise types. This tactic carries the risk of severe harmful health effects, including liver injury. Most anabolic-androgenic steroid stacking protocols employed are based on the use of the ‘prototypic’ anabolic-androgenic steroid testosterone and/or its esters. There is a vast body of data on the effects of anabolic-androgenic steroids’ abuse combined with physical exercise training on the liver antioxidant barrier in adult subjects, whereas those concerning adolescents are scant. This study aimed to assess, in adolescent male Wistar rats undergoing a 6-week moderate-intensity endurance training (treadmill running), the influence of concurrent weekly supplementation with intramuscular testosterone enanthate (TE, 8 or 80 mg/kg body weight/week) on selected indices of liver status and oxidative stress. The rats were sacrificed, and their livers and blood samples were harvested two days after the last training session. High-dose TE treatment significantly reduced body and liver weight gains. Neither low-dose nor high-dose TE treatment affected liver α-tocopherol or γ-tocopherol content, whereas low-dose TE treatment significantly lowered hepatic reduced glutathione content. TE treatment significantly elevated liver thiobarbituric acid-reactive substances content and blood activities of alkaline phosphatase and γ-glutamyltransferase, but not of aspartate aminotransferase or alanine aminotransferase. Liver catalase activity was lowered by >50% in both TE-treated groups, while superoxide dismutase activity was significantly but slightly affected (−15%) only by the high-dose TE treatment. Glutathione peroxidase and glutathione reductase activities were not significantly altered. TE treatment significantly increased liver thiobarbituric acid-reactive substances content and lowered blood HDL-cholesterol, but did not significantly affect LDL-cholesterol or triglycerides level. In conclusion, high-dose TE treatment significantly disturbed liver antioxidant barrier and prooxidative-antioxidative balance and hence counteracted favorable effects of concurrent moderate-intensity endurance training in adolescent male rats.
“…The higher TE dose significantly lowered BW gain and LW as compared to those in TE-untreated EndTr rats, but caused no substantial shift in the LW/BW ratio (−5%, p = 0.66) and thus no apparent hepatotoxicity in EndTr rats. Earlier, we found a significantly reduced LW/BW ratio in high-dose TE-treated adolescent UTr rats (Sadowska-Krępa et al, 2017), which may have been due to the start of TE treatment at a younger age. The training was performed at an intensity that allows maximal fat oxidation (Purdom et al, 2018), and the mean BW gains were less in all three EndTr groups than in the respective UTr groups, see Sadowska-Krępa et al (2017).…”
Section: Discussionmentioning
confidence: 55%
“…All biochemical determinations in blood serum and liver samples, except for serum lipids that were not determined before, were performed as described earlier (Sadowska-Krępa et al, 2017). Specifically: The total serum testosterone (TT) level was assessed with a DSL-4100 Testosterone RIA Kit (Diagnostic Systems Laboratories, Webster, TX, USA).…”
Section: Assay Methodsmentioning
confidence: 99%
“…All other data were analyzed by a one-way ANOVA with weekly TE dose as the main factor, followed by the Tukey test when appropriate. Comparisons with data from our previous study (Sadowska-Krępa et al, 2017) were made using Student's t -test for independent variables, as indicated in the text. Associations between variables were assessed using the Spearman rank correlation test.…”
Section: Endtr Endtr+te8 Endtr+te80mentioning
confidence: 99%
“…Our earlier study on the effects of long-term testosterone treatment on the liver antioxidant barrier and some blood markers of liver injury in sedentary adolescent male rats showed some signs of enhanced liver oxidative stress and toxicity but no potential lasting harm (Sadowska-Krępa et al, 2017). Here, we tested the possible harmful effects of this treatment in a situation aimed to model androgen abuse to aid physical exercise training.…”
In some countries, anabolic-androgenic steroid abuse is rampant among adolescent boys and young men, including some of those seeking physical fitness and/or pleasing appearance through various exercise types. This tactic carries the risk of severe harmful health effects, including liver injury. Most anabolic-androgenic steroid stacking protocols employed are based on the use of the ‘prototypic’ anabolic-androgenic steroid testosterone and/or its esters. There is a vast body of data on the effects of anabolic-androgenic steroids’ abuse combined with physical exercise training on the liver antioxidant barrier in adult subjects, whereas those concerning adolescents are scant. This study aimed to assess, in adolescent male Wistar rats undergoing a 6-week moderate-intensity endurance training (treadmill running), the influence of concurrent weekly supplementation with intramuscular testosterone enanthate (TE, 8 or 80 mg/kg body weight/week) on selected indices of liver status and oxidative stress. The rats were sacrificed, and their livers and blood samples were harvested two days after the last training session. High-dose TE treatment significantly reduced body and liver weight gains. Neither low-dose nor high-dose TE treatment affected liver α-tocopherol or γ-tocopherol content, whereas low-dose TE treatment significantly lowered hepatic reduced glutathione content. TE treatment significantly elevated liver thiobarbituric acid-reactive substances content and blood activities of alkaline phosphatase and γ-glutamyltransferase, but not of aspartate aminotransferase or alanine aminotransferase. Liver catalase activity was lowered by >50% in both TE-treated groups, while superoxide dismutase activity was significantly but slightly affected (−15%) only by the high-dose TE treatment. Glutathione peroxidase and glutathione reductase activities were not significantly altered. TE treatment significantly increased liver thiobarbituric acid-reactive substances content and lowered blood HDL-cholesterol, but did not significantly affect LDL-cholesterol or triglycerides level. In conclusion, high-dose TE treatment significantly disturbed liver antioxidant barrier and prooxidative-antioxidative balance and hence counteracted favorable effects of concurrent moderate-intensity endurance training in adolescent male rats.
“…Ischemic pre-conditioning and post-conditioning can induce increased expression of Hsp 27, which can protect the tissue from ischemia reperfusion injury, thus constituted an endogenous protective mechanism. Studies have reported that Hsp 27 can protect cerebral ischemia reperfusion injury (Sadowska-Krępa et al, 2017), increased Hsp 27 could reduce azithromycin-induced cardiac cell death (Kumar et al, 2016), and Hsp 27 can alleviate cerebral ischemia reperfusion injury (Mohammadi-Ostad-Kalayeh et al, 2017). This research found that, compared with the ischemic control group, Hsp 27 and Hsp 27 levels increased significantly after medication, suggesting that the protective effect of Antelope horn on cerebral ischemia reperfusion is correlated with the elevation of Hsp 27 and Hsp 70.…”
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